萘丁美酮对小鼠免疫功能的影响

目的 :研究萘丁美酮对小鼠免疫功能的影响。方法 :小鼠灌胃萘丁美酮后 ,分别观察胸腺、脾脏重量 ,腹腔巨噬细胞吞噬功能和游走功能 ,体内PHA诱导的淋巴细胞转化。结果 :萘丁美酮能明显减轻小鼠胸腺和脾脏重量 ,降低小鼠腹腔巨噬细胞吞噬游走功能 ,抑制PHA诱导的小鼠淋巴细胞转化。结论 :萘丁美酮对小鼠细胞免疫功能有明显的抑制作用。     

911-FITC荧光探针与免疫细胞的结合实验

应用911-FJTC荧光探针对胸腺、脾脏淋巴细胞、巨噬细胞和内皮细胞进行了荧光染色，采用流式细胞仪及荧光显微镜对细胞的染色情况进行了评价。结果表明，911-FITC荧光探针能与淋巴细胞、巨噬细胞和内皮细胞发生特异性结合。证明911可通过与免疫细胞直接结合而起到免疫调节作用。     

罗汉果多糖对小鼠免疫功能的影响

目的研究罗汉果多糖(SGPS1)对小鼠免疫功能的影响。方法测定小鼠胸腺指数、脾脏指数、腹腔巨噬细胞吞噬功能、血清溶血素形成和淋巴细胞转化率。结果SGPS1在高、低剂量下均明显使小鼠胸腺、脾脏等免疫器官重量增加;使小鼠腹腔巨噬细胞吞噬鸡红细胞百分率及吞噬指数增加;提高小鼠血清溶血素水平;增加小鼠淋巴细胞转化率及胸腺、脾脏指数。结论SGPS1有增强机体免疫功能的作用。     

壳寡糖与D-氨基葡萄糖盐酸盐体外对小鼠淋巴细胞和腹腔巨噬细胞作用的比较

目的：观察壳寡糖和D-氨基葡萄糖盐酸盐(GAH)体外对小鼠免疫细胞作用。方法：应用MTT法观察体外壳寡糖和GAH对小鼠脾淋巴细胞细胞增殖的影响,应用巨噬细胞吞噬中性红试验观察壳寡糖和GAH对小鼠腹腔巨噬细胞吞噬功能的影响。结果：GAH浓度在200、100mg·L~(-1)时,能显著促进GonA诱导的小鼠脾细胞增殖,壳寡糖浓度为200、40mg·L~(-1)时,能增强小鼠腹腔巨噬细胞的吞噬能力。结论：结果表明壳寡糖和GHA对免疲细胞的调节作用是通过不同的途径实现的。     

合成鱼腥草素对环磷酰胺模型小鼠免疫功能的影响

对于环磷酰胺所致免疫功能低下模型小鼠 ,灌胃给予合成鱼腥草素 6 0mg/kg、12 0mg/kg能明显增加环磷酰胺所致免疫功能低下模型小鼠的脾脏指数、外周血淋巴细胞ANAE阳性百分率 ;增强单核巨噬细胞吞噬功能、迟发型超敏反应强度及ConA诱导的脾脏T淋巴细胞增殖能力 ;对胸腺指数则无明显影响 ;合成鱼腥草素 12 0mg/kg还能明显增强环磷酰胺模型小鼠血清溶血素的生成及脾脏空斑形成细胞溶血能力 .     

茶多酚对D-半乳糖致衰老小鼠免疫功能的调节作用

目的:观察茶多酚对D-半乳糖致衰老小鼠免疫功能的调节作用。方法:昆明种小鼠随机分为正常对照组、衰老模型组和茶多酚低、中、高剂量模型给药组,3个剂量组每天分别按1.0,2.0,4.0g.kg-1.d-1灌胃,正常对照组和模型组均灌胃等量生理盐水溶液,连续30d。计算胸腺与脾脏指数,测定淋巴细胞转化能力、小鼠腹腔巨噬细胞吞噬功能和外周血IL-2水平。结果:D-半乳糖致衰老小鼠免疫功能明显下降,表现为胸腺与脾脏指数、淋巴细胞转化能力、腹腔巨噬细胞吞噬功能、外周血IL-2含量均明显降低(P<0.05,P<0.01);茶多酚能提高模型小鼠胸腺与脾脏指数、淋巴细胞转化能力、腹腔巨噬细胞吞噬功能和外周血IL-2含量(P<0.05,P<0.01)。结论:茶多酚明显增强D-半乳糖致衰老小鼠的免疫机能,是一种免疫调节剂。     

甲壳胺胶囊对小鼠免疫功能的影响

目的探讨甲壳胺胶囊对小鼠免疫功能的影响。方法免疫实验采用0.045、0.45、1.35g/kg剂量的甲壳胺胶囊,小鼠经口灌胃30d,分别测定免疫器官脏器/体质量比值、半数溶血值、抗体生成细胞数、ConA诱导的小鼠脾淋巴细胞转化实验、迟发型变态反应和碳廓清实验、小鼠腹腔巨噬细胞吞噬鸡红细胞实验、NK细胞活性。结果与阴性对照组比较,1.35g/kg剂量能提高小鼠的半数溶血值(HC50)、小鼠抗体生成细胞数,1.35、0.45g/kg剂量能增强小鼠的迟发型变态反应能力。3个剂量对小鼠体质量增长、胸腺体质量比值、脾脏体质量比值、小鼠单核-巨噬细胞碳廓清能力、Co-nA诱导的小鼠脾淋巴细胞转化能力、小鼠腹腔巨噬细胞吞噬鸡红细胞的能力、NK细胞活性均无影响。结论甲壳胺胶囊有增强免疫力的作用。     

芦荟凝胶原汁及其多糖提取物对小鼠免疫功能的影响

目的 研究芦荟凝胶原汁及其多糖对小鼠免疫功能的影响。方法 芦荟凝胶原汁及其多糖饲喂小鼠,测定各组小鼠的脾脏和胸腺重量、巨噬细胞吞噬功能及淋巴细胞数量与功能。结果 与对照组相比芦荟凝胶原汁及其多糖溶液均使小鼠免疫器官脾脏、胸腺重量有不同程度的增加;小鼠腹腔巨噬细胞的吞噬百分数分别从17.33％增长至53.17％和38.57％,吞噬指数分别从0.28增长至1.23和0.69;与对照组相比小鼠外周血液中的T淋巴细胞数量和功能也有显著增加。结论 初步说明两者对小鼠的机体免疫功能均有一定的增强作用,且效果前者优于后者。     

海藻硫酸多糖对小鼠免疫功能的调节作用

目的：观察海藻硫酸多糖（SPS）对正常小鼠和免疫低下小鼠免疫功能的调节作用。方法：测定小鼠腹腔巨噬细胞吞噬鸡红细胞的能力、碳粒廓清能力、血清溶血素形成,,并进行二硝基氟苯诱导小鼠迟发性变态反应实验、T,B淋巴细胞增殖实验,考察SPS对正常小鼠免疫功能的影响;测定环磷酰胺致免疫低下小鼠的血象、胸膜指数和T淋巴细胞亚群,进行T,B淋巴细胞增殖实验,考察SPS对免疫低下小鼠免疫功能的影响。结果：SPS能增强正常小鼠腹腔巨噬细胞吞噬鸡红细胞的能力,高剂量SPS能增强小鼠碳粒廓清能力,高、中剂量SPS能提高小鼠血细胞凝集程度,SPS体外对T,B淋巴细胞有促增殖作用。对于环磷酰胺所致免疫低下小鼠,SPS可以通过调节血象、增加胸腺指数、提高T淋巴细胞和CD8^ 细胞数目、促进T,B淋巴细胞增殖来缓解小鼠免疫功能的低下。结论：SPS是一种免疫调节剂,具有免疫调节和抗病毒作用,是新一代抗HIV药物的发展方向。     

双氯灭痛对小鼠免疫功能的影响

双氯灭痛按25mg/kg和50mg/kg两种剂量每天灌胃1次,连续4～5d。结果表明,(1) 双氯灭痛可降低小鼠腹腔巨噬细胞对鸡红细胞的吞噬率和吞噬指数;(2) 在免疫抑制状态下,降低小鼠腹腔巨噬细胞对鸡红细胞的吞噬率和吞噬指数更明显;(3) 降低鸡红细胞致敏小鼠的溶血素形成;(4) 能使鸡红细胞致敏小鼠胸腺重量明显减轻,但使脾脏增重;(5) 对PHA诱导的小鼠外周血淋巴细胞转化呈促进作用。     

Immunological and anti-inflammatory effects of clarithromycin: inhibition of interleukin 1 production of murine peritoneal macrophages

The immunological and anti-inflammatory effects of clarithromycin (CAM), a new oral macrolide antibiotic, were examined in in vitro models such as lymphocyte transformation (LTF) of murine spleen cells, interleukin 1 (IL-1) production of murine peritoneal macrophages and IL-1-induced proliferation of C3H/HeJ mice thymocytes; the results were compared with those achieved by erythromycin (EM). CAM suppressed these responses much more than EM. Murine peritoneal macrophages precultured with CAM showed diminished IL-1 production, but macrophages precultured with EM did not, indicating that CAM has suppressive effects on the early phase of IL-1 production of murine peritoneal macrophages. Suppressive effects of CAM on IL-1 production by macrophages and proliferation of lymphocytes were independent of prostaglandin biosynthesis, since this drug had no effect on cyclooxygenase activity. Additional immunosuppressive and anti-inflammatory activities of CAM may explain its superior clinical effect.     

Immunomodulatory activity of polysaccharides isolated from Strongylocentrotus nudus eggs

Our previous work showed that SEP, a novel glucan isolated from the eggs of sea urchins, Strongylocentrotus nudus, had remarkable anti-tumor activity. To elucidate the mechanism of the anti-tumor activity, the immunomodulatory activity of SEP was investigated. The in vivo experiment results showed that SEP remarkably enhanced spleen and thymus index in S180-bearing mice, and also stimulated ConA-induced splenocyte proliferation. Immunomodulatory activity assay in vitro indicated SEP could significantly enhance the mouse splenocyte proliferation in a dose-dependent manner. According to comitogenic activity tests, SEP showed significant comitogenic activities and adjuvant properties. We also demonstrated that SEP had a unique mode of immunostimulation with regard to its cell-type specificity. In other words, SEP markedly stimulated B and T cell proliferation, however the influence on B cells was greatly weaker than that on T cells. IL-2, TNF-alpha, and IFN-gamma mRNA expression was upregulated after the mouse splenocytes were treated by SEP, indicating that Th1 cell was the primary cellular target affected by SEP on T lymphocyte. SEP enhanced production of nitric oxide (NO), upregulated mRNA expression of inducible nitric oxide synthase (iNOS) in peritoneal macrophages in a dose-dependent manner. In addition, SEP did not show direct toxicity to tumor cells. Consequently, the anti-tumor effect of SEP was related to stimulating host immunity/enhancing the immune system functions, which may mainly result from SEP activating lymphocytes and macrophages and stimulating secretion of some cytokines.     

Regulation of methionine enkephalin on the function of lymphocytes and macrophages from liver-impaired mice

测定了甲硫脑啡肽对肝损伤小鼠淋巴细胞和巨噬细胞的效应．结果显示肝损伤能够显著地抑制淋巴细胞的增殖反应，甲硫脑啡肽可以减轻这种抑制作用．甲硫脑啡肽也提高肝损伤组淋巴细胞的电泳率，这提示淋巴细胞表面电荷的改变．巨噬细胞移动抑制实验的数据提示甲硫脑啡肽能够显著地抑制巨噬细胞移动抑制因子与巨噬细胞结合．实验结果表明甲硫脑啡肽对免疫细胞功能起重要调节作用．     

甲硫脑啡肽对肝损伤小鼠淋巴细胞和巨噬细胞功能的调节作用

测定了甲硫脑啡肽对肝损伤小鼠淋巴细胞和巨噬细胞的效应. 结果显示肝损伤能够显著地抑制淋巴细胞的增殖反应，甲硫脑啡肽可以减轻这种抑制作用. 甲硫脑啡肽也提高肝损伤组淋巴细胞的电泳率，这提示淋巴细胞表面电荷的改变. 巨噬细胞移动抑制实验的数据提示甲硫脑啡肽能够显著地抑制巨噬细胞移动抑制因子与巨噬细胞结合. 实验结果表明甲硫脑啡肽对免疫细胞功能起重要调节作用.     

角燕制剂对小鼠免疫功能的调节作用

目的观察角燕提取物对小鼠免疫功能的影响。方法采用盐溶液提取、有机溶剂分级沉淀等步骤 ,从角燕的有效部位中制备得到角燕制剂 ,用不同剂量的制剂给小鼠灌胃 ,观察其对小鼠免疫功能的调节作用。结果角燕制剂能显著提高小鼠的胸腺指数和脾指数 ,促进淋巴细胞转化 ,增强小鼠NK细胞杀伤活性及腹腔巨噬细胞的吞噬活性。结论角燕制剂能明显提高机体的免疫功能 ,提示也是其抑瘤作用机制之一     

低氧暴露对小鼠脾淋巴细胞增殖和凋亡的影响

目的 研究低氧暴露诱导淋巴细胞数量减少与细胞增殖和凋亡的关系。方法 从C57BL/6小鼠脾中分离淋巴细胞,将淋巴细胞分别在低氧（1%O₂）和常氧（21%O₂）环境中培养12、24、48 h。用流式细胞术检测T、B淋巴细胞数量;羧基荧光素乙酰乙酸和AnnexinⅤ-FITC/PI方法分别检测淋巴细胞的增殖和凋亡;扫描电镜观察淋巴细胞形态;实时荧光定量逆转录PCR和Western blot检测凋亡相关因子鼠源B细胞淋巴瘤/白血病-2（bcl-2）、bcl-2同源拮抗剂-杀伤蛋白（Bak）和胱天蛋白酶-3（caspase-3）的mRNA和蛋白表达水平。结果 低氧暴露12、24、48h,可降低T、B淋巴细胞数量,抑制淋巴细胞增殖,促进细胞凋亡;扫描电镜观察显示,同一时间下,低氧组淋巴细胞更早出现凋亡特征形态学变化;低氧暴露12、24、48 h,淋巴细胞Bak和caspase-3的mRNA和蛋白表达水平均上调,而bcl-2的mRNA和蛋白表达水平均下调。结论 低氧暴露通过抑制淋巴细胞增殖、促进凋亡,从而介导淋巴细胞数量下降。     

七叶皂苷体外抗SGC-7901细胞的作用及机制研究

目的研究七叶皂苷体外抗SGC-7901肿瘤细胞的作用及其机制。方法采用MTT法观察药物对SGC-7901肿瘤细胞的增殖抑制作用;采用流式细胞仪检测SGC-7901肿瘤细胞周期的变化;FITC-AnnexinⅤ/PI双标记检测SGC-7901肿瘤细胞的凋亡;Western blot检测凋亡相关蛋白Bcl-2的表达。结果七叶皂苷可明显抑制SGC-7901肿瘤细胞的增殖,并抑制细胞周期和诱导细胞发生凋亡,可下调凋亡相关蛋白Bcl-2的表达。结论七叶皂苷体外对SGC-7901肿瘤细胞具有良好的抑制作用,并可诱导细胞发生凋亡。     

红车轴草提取物对小鼠淋巴细胞活化与增殖及巨噬细胞分泌NO的影响

探讨红车轴草提取物(RCE)在体外对小鼠T淋巴细胞和巨噬细胞的影响。MTT法检测RCE对细胞的毒性作用。荧光抗体染色结合流式细胞术检测RCE对T淋巴细胞在Con A的刺激下表达活化抗原CD69、CD25、CD71的影响。CFDA-SE标记技术结合流式细胞术分析RCE对T淋巴细胞在Con A诱导下增殖情况的影响。Griess法检测RCE对小鼠巨噬细胞在LPS刺激24 h后分泌NO的影响。RCE对小鼠有潜在的抗炎作用。RCE对小鼠淋巴细胞和巨噬细胞的细胞毒作用很小。不同质量浓度的RCE能够很好的抑制过量的炎症相关信号分子表达，如NO, CD69, CD25, CD71，且呈剂量依赖性。RCE能够抑制T淋巴细胞的增殖。数据显示RCE可能通过对小鼠淋巴细胞活化与增殖及巨噬细胞NO分泌的抑制展示其抗炎效应。     

LNP 906, the first high-affinity photoaffinity ligand selective for I1 imidazoline receptors

1 The hypotensive effect of imidazoline-like drugs, such as clonidine, was attributed both to alpha2-adrenergic receptors and nonadrenergic imidazoline receptors, which are divided into I1, I2 and I3 subtypes. 2 We have recently synthesized a derivative of (2-(2-chloro-4-iodo-phenylamino)-5-methyl-pyrroline (LNP 911), the first high-affinity and selective ligand for I1 receptors (I1R), with a photoactivable function (LNP 906). 3 This work aims to test whether this derivative retained the binding properties of LNP 911 and bound irreversibly to I1R. 4 Binding studies showed that LNP 906 exhibited nanomolar affinity for I1R and was selective for I1R over I2 receptors and alpha2-adrenergic receptors (alpha2Ars). 5 Upon exposure to u.v. light, LNP 906 irreversibly blocked the binding of [125I]-paraiodoclonidine (PIC) to I1R, time- and dose-dependently, on PC12 cell membranes and interacted with I1R in a reversible and competitive manner in the absence of light. Pharmacological studies showed that this blockade was prevented by the concomitant presence of rilmenidine (a well-known I1 agonist), but not by rauwolscine (an alpha2 antagonist). 6 Finally, LNP 906 clearly antagonized the decrease in forskolin-stimulated cAMP level induced by rilmenidine, but not by melatonin. 7 These results indicate that LNP 906 is the first high-affinity and selective photoaffinity ligand for I1R and that it behaves as an I1R antagonist.